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Results for “MESENTERIC VESSELS”

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At least 127 records · Page 7Linked to original sources
PubMed1987

The rationale for "second-look operation" in mesenteric vessel occlusion with uncertain intestinal viability at primary surgery.

In a 10-year period, 80 patients, median age 78 years, were operated on for mesenteric vascular occlusion--arterial in 50 cases, venous in 24 and of uncertain etiology in six cases. Abdominal pain out of proportion to physical findings occurred in only eight cases. Vague abdominal symptoms with increasing tenderness led to surgical exploration in most cases. Median patient delay was 34 hours and doctor's delay 15 hours. Resection was primarily nonfeasible in 28 cases. Primary resection without second-look operation was performed in 32 cases, in seven of which signs of anastomotic insufficiency appeared. In the remaining 20 cases, primary resection (18) and/or embolectomy (3/2) was followed by a planned second-look operation within 24 hours, when five resections were performed. In a patient with viable anastomosis at second look, there were late signs of anastomotic insufficiency. Although the data do not permit firm recommendations, use of second-look operation in patients with doubtful viability of the intestine may reduce the extent of resection at primary exploration and also the incidence of insufficient anastomosis.

Adult↗
PubMed1989

Bunazosin, an alpha 1-adrenoceptor blocker, differentially releases co-transmitters in dog mesenteric vessels.

The effects of bunazosin on the electrical and mechanical responses of smooth muscle cells elicited by exogenously applied noradrenaline (NA) and by perivascular nerve stimulation were studied in the isolated mesenteric artery and vein of the dog. NA (above 10(-7) M in the artery and above 3 X 10(-8) M in the vein) depolarized the membrane. Perivascular nerve stimulation evoked an excitatory junction potential (e.j.p.) and slow depolarization in both vessels. Bunazosin and prazosin inhibited the NA-induced depolarization and slow depolarization in the artery but not in the vein. The NA actions in the vein were inhibited by yohimbine. Bunazosin (above 10(-6) M) increased the amplitude of the e.j.p. but decreased the outflow of NA during nerve stimulation. The amplitude and conduction velocity of the compound action potential of perivascular nerves were inhibited by higher concentrations of bunazosin (above 10(-5) M). The results provide evidence that bunazosin has selective inhibitory actions at alpha 1-adrenoceptors. This drug exerted differential effects on the release of co-transmitters which generate the e.j.p. and the slow depolarization, as bunazosin increased the former and decreased the latter. This suggests that e.j.p. is generated by a substance other than NA.

Action Potentials↗
PubMed1979

[Pathomorphological changes and the level of intestinal resection in acute occlusion of the mesenteric vessels].

The analysis of 239 case histories and of 229 autopsy recores of patients died from this disease in set forth in the article. The ratio of mesenteric thrombosis and embolism constituted 2.78% of all the autopsies. The occlusion of the superior mesenteric artery was found in 76.0% of all the autopsies, of the mesenteric veins--in 14.7%, of the inferior mesenteric artery--in 4.2%, of both superior and inferior mesenteric arteries--in 4.2% and of the celiac and superior mesenteric arteries--in 0.83%.

Acute Disease↗
PubMed1996

Role of endothelium in the abnormal response of mesenteric vessels in rats with portal hypertension and liver cirrhosis.

BACKGROUND & AIMS: Previous studies have shown that nitric oxide synthesis inhibition corrects the hyporesponsiveness to vasoconstrictors present in the mesenteric vascular bed of portal-hypertensive rats. The origin of this elevated NO production, whether endothelial or muscular, is unknown. The aim of this study was to evaluate the role of vascular endothelium in the hyporesponsiveness to methoxamine (MTX) in the mesenteric vascular bed of portal vein-ligated (PVL) and cirrhotic rats. METHODS: Endothelial denudation was achieved using a combined treatment of cholic acid and distilled water. RESULTS: Compared with the respective control groups, PVL rats showed a reduced vascular response to MTX. Similar results were obtained in cirrhotic animals. The presence of ascites was associated with a more severe reduction in the response to MTX. Removal of the endothelium completely corrected the vascular hyporesponsiveness of PVL, cirrhotic nonascitic, and ascitic animals. In these experiments, acetylcholine-mediated vasodilation was practically absent whereas that of sodium nitroprusside was potentiated, which indicates a successful elimination of the endothelium and the preservation of smooth muscle function. Immunostaining for NO synthase isoforms revealed the presence of endothelial NO synthase protein in healthy and PVL rats exclusively in the endothelium. CONCLUSIONS: The mesenteric vascular hyporesponsiveness to MTX present in these models of liver diseases and portal hypertension is solely due to endothelium-dependent factors.

Animals↗